Sodeyama N, Ishida K, Jaeckle K A, Zhang L, Azuma A, Yamada M, Mizusawa H, Wada Y
Department of Neurology, Tokyo Medical and Dental University, Japan.
J Neurol Neurosurg Psychiatry. 1999 Jan;66(1):97-9. doi: 10.1136/jnnp.66.1.97.
Previous study has shown that the anti-Hu antibody titre of serum samples from patients with paraneoplastic encephalomyelitis/paraneoplastic sensory neuronopathy (PEM/PSN) was significantly higher than that from patients with small cell lung cancer without neurological disturbances (non-PEM/PSN). The aims of this study were (1) to identify the fine epitopes on HuD recognised by the anti-Hu antibody, (2) to determine if the pattern of epitopic reactivity differed between antibodies from patients with and without PEM/PSN, and (3) to determine if the pattern of epitopic reactivity correlated with the clinical features. Recombinant full length HuD and nine deletion fragments were constructed and immunoreacted by western blot analysis with 14 anti-Hu serum samples from eight patients with PEM/PSN and six without PEM/IPSN. All anti-Hu serum samples reacted with the deletion fragments containing amino acids (aa) 90-101 or aa 171-206. Some anti-Hu samples reacted with the deletion fragments containing aa 223-234, aa 235-252, or aa 354-373. There was no difference in the pattern of epitopic reactivity between patients with and without PEM/PSN. There was no correlation between the pattern of epitopic reactivity and the clinical features. The anti-Hu antibody titre from patients with PEM/ PSN was significantly higher than from patients without PEM/PSN, but there was overlap of their titre concentrations. In conclusion, aa 90-101 and aa 171-206 are the major epitopes with which all anti-Hu serum samples react, and aa 223-234, aa 235-252, and aa 354-373 are the minor epitopes with which only some anti-Hu serum samples react. The analyses suggested that the pattern of epitopic reactivity of the anti-Hu antibody on HuD was not a critical factor for the development or clinical features of PEM/PSN.
先前的研究表明，副肿瘤性脑脊髓炎/副肿瘤性感觉神经元病（PEM/PSN）患者血清样本中的抗Hu抗体滴度显著高于无神经功能障碍的小细胞肺癌患者（非PEM/PSN）。本研究的目的是：（1）鉴定抗Hu抗体识别的HuD上的精细表位；（2）确定有或无PEM/PSN患者的抗体之间表位反应性模式是否不同；（3）确定表位反应性模式是否与临床特征相关。构建了重组全长HuD和9个缺失片段，并通过蛋白质印迹分析与来自8例PEM/PSN患者和6例无PEM/IPSN患者的14份抗Hu血清样本进行免疫反应。所有抗Hu血清样本均与包含氨基酸（aa）90-101或aa 171-206的缺失片段发生反应。一些抗Hu样本与包含aa 223-234、aa 235-252或aa 354-373的缺失片段发生反应。有或无PEM/PSN患者之间的表位反应性模式没有差异。表位反应性模式与临床特征之间没有相关性。PEM/PSN患者的抗Hu抗体滴度显著高于无PEM/PSN患者，但其滴度浓度存在重叠。总之，aa 90-101和aa 171-206是所有抗Hu血清样本均与之反应的主要表位，aa 223-234、aa 235-252和aa 354-373是仅部分抗Hu血清样本与之反应的次要表位。分析表明，抗Hu抗体在HuD上的表位反应性模式不是PEM/PSN发生或临床特征的关键因素。
